To further assess the relevance of this SHH/AMPK/CNBP axis in SHH medulloblastoma, we investigated the level of protein expression of CNBP in both normal and tumorigenic cerebellums in the presence or in the absence of AMPKα2. We observed that, in both physiological (SmoA1−) and pathophysiological (SmoA1+) contexts, the loss of AMPKα2 resulted in lower levels of the CNBP protein (Figure 3a). This evidence concerns the gene PRKAA1 and medulloblastoma.